LINC01234 通过调节 miR-637/NUPR1 轴促进口腔鳞状细胞癌的生长和侵袭。
LINC01234 facilitates growth and invasiveness of oral squamous cell carcinoma through regulating the miR-637/NUPR1 axis.
机构信息
Department of Pediatric Dentistry, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Department of Oncology Surgery, General Hospital of Heilongjiang Province Land Reclamation Bureau, Harbin, 150000, China.
出版信息
Biomed Pharmacother. 2019 Dec;120:109507. doi: 10.1016/j.biopha.2019.109507. Epub 2019 Oct 4.
LINC01234 plays a pivot role in the tumorigenesis of gastric cancer, colon cancer and lung cancer. However, how LINC01234 participates in oral squamous cell carcinoma (OSCC) progression remains unknown. In our research, we showed that LINC01234 was dramatically upregulated in OSCC tissues. And interestingly, high LINC01234 expression predicted a low overall survival rate in OSCC patients. Knockdown of OSCC inhibited the proliferation of cancer cells and led to more cells restricted in G0 phase. Moreover, LINC01234 silencing decreased the migration and invasion of OSCC cells. Additionally, downregulation of LINC01234 limited OSCC tumor propagation in vivo. Mechanistic investigation elucidated that LINC01234 inhibited the activity of miR-637 to increase the expression of NUPR1. Via upregulating NUPR1 level, LINC01234 contributed to malignant behaviors of OSCC cells. Collectively, our research shows that LINC01234 exerts an important role in OSCC progression via miR-637/NUPR1 axis.
LINC01234 在胃癌、结肠癌和肺癌的肿瘤发生中发挥着关键作用。然而，LINC01234 如何参与口腔鳞状细胞癌（OSCC）的进展尚不清楚。在我们的研究中，我们表明 LINC01234 在 OSCC 组织中显著上调。有趣的是，高表达 LINC01234 预示着 OSCC 患者的总体生存率较低。敲低 OSCC 抑制了癌细胞的增殖，并导致更多的细胞停滞在 G0 期。此外，LINC01234 的沉默减少了 OSCC 细胞的迁移和侵袭。此外，下调 LINC01234 限制了 OSCC 肿瘤在体内的传播。机制研究表明，LINC01234 抑制 miR-637 的活性，从而增加 NUPR1 的表达。通过上调 NUPR1 水平，LINC01234 促进了 OSCC 细胞的恶性行为。总之，我们的研究表明，LINC01234 通过 miR-637/NUPR1 轴在 OSCC 进展中发挥重要作用。
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